This proposal is a request for an ADAMHA RSDA level II support for Gerald D. Frye, Ph.D. and closely related to R01 AA06322 on which Dr. Frye is the PI. This award will allow Dr. Frye's responsibilities for University and Department service and teaching to be reduced so that he will be able to apply at least 90% of his time to research and professional development. Those departmental resources that are no longer required for Dr. Frye's support will be used to recruit an additional faculty member with biochemical research interests related to alcohol and drug abuse questions. Dr. Frye's research efforts will continue to focus on the role that GABAA and GABAB receptor/transducer complexes play in the genesis of ethanol intoxication, tolerance and physical dependence. The hypothesis being tested is that, "acute or chronic actions of ethanol depend in part on increased or decreased efficacy of GABA receptors, respectively, as synaptic transducers". Studies are designed to evaluate the influence of ethanol treatment on the physiology of model GABAA and GABAB receptor systems. Not only will Dr. Frye continue his research using the guinea pig ileum but he will broaden his research training by learning new neurophysiological techniques in the rat hippocampal slice through an important collaboration with Dr. William Griffith. Additional opportunities for training and new research should come form other planned collaborations in areas where a GABA receptor-ethanol interaction could be an underlying cause of ethanol toxicity. In this regard preliminary collaborations with Dr. Kelly Hester (cardiovascular physiology and hypertension); Dr. Jack Nations (heavy metals toxicity and ethanol preference); and and individual yet to be hired by the Department (ion channel biochemistry). These plans for new training and increased interdisciplinary research collaboration should significantly enhance Dr. Frye's professional development as a basic scientist interested in the biomedical impact of ethanol.